Abstract
It has been proposed that thiazide-induced kaliuresis results from aldosterone activity stimulated by sodium depletion. In studies in adrenalectomized dogs, chlorothiazide produced a significant kaliuresis, indicating that mineralocorticoid activity is not necessary for this effect. Comparison of the kaliuresis from chlorothiazide with that from bendroflumethiazide (which has minimal carbonic anhydrase activity) indicates that carbonic anhydrase inhibition is not necessary. Thus the kaliuresis resulting from the thiazide diuretics is probably the result of increased distal tubular secretion dependent upon increased availability of sodium, although an effect of inhibition of proximal tubular rabsorption of potassium has not been ruled out.
Footnotes
- Received January 5, 1966.
- Accepted January 9, 1967.
- © 1967 by The Williams & Wilkins Company
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